c o r t e x 7 5 ( 2 0 1 6 ) 1 9 3 e2 0 3
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Phonetic basis of phonemic paraphasias in
aphasia: Evidence for cascading activation
Kathleen Kurowski and Sheila E. Blumstein*
Department of Cognitive Linguistic & Psychological Sciences, Brown University, Providence, RI United States
article info
abstract
Article history:
Phonemic paraphasias are a common presenting symptom in aphasia and are thought to
Received 31 August 2015
reflect a deficit in which selecting an incorrect phonemic segment results in the clear-cut
Reviewed 12 October 2015
substitution of one phonemic segment for another. The current study re-examines the
Revised 16 November 2015
basis of these paraphasias. Seven left hemisphere-damaged aphasics with a range of left
Accepted 18 December 2015
hemisphere lesions and clinical diagnoses including Broca's, Conduction, and Wernicke's
Action editor Cynthia Thompson
aphasia, were asked to produce syllable-initial voiced and voiceless fricative consonants,
Published online 31 December 2015
[z] and [s], in CV syllables followed by one of five vowels [i e a o u] in isolation and in a
carrier phrase. Acoustic analyses were conducted focusing on two acoustic parameters
Keywords:
signaling voicing in fricative consonants: duration and amplitude properties of the fricative
Phonemic paraphasias
noise. Results show that for all participants, regardless of clinical diagnosis or lesion site,
Aphasia
phonemic paraphasias leave an acoustic trace of the original target in the error production.
Acoustic trace
These findings challenge the view that phonemic paraphasias arise from a mis-selection of
Cascading activation
phonemic units followed by its correct implementation, as traditionally proposed. Rather,
they appear to derive from a common mechanism with speech errors reflecting the coactivation of a target and competitor resulting in speech output that has some phonetic
properties of both segments.
© 2015 Elsevier Ltd. All rights reserved.
1.
Introduction
Historically, the study of speech errors in both normal and
aphasic populations has informed and challenged theories of
the processes involved in spoken word production. In the
study of normal populations, speech errors have been viewed
as providing evidence for the psychological reality of phonemes and phonological features, which in turn has been
used to support various stages of speech production. Here,
production of a word is considered to be a serial process
* Corresponding author.
E-mail address: [email protected] (S.E. Blumstein).
http://dx.doi.org/10.1016/j.cortex.2015.12.005
0010-9452/© 2015 Elsevier Ltd. All rights reserved.
occurring in separate stages, with the sound shape of a lexical
entry accessed, followed by phonological planning, and ultimately articulatory implementation. Speech production
models based on speech errors in normals (cf. Meyer, 1992)
located most speech errors at the phonological planning level,
thereby taking into account the fact that (a.) most sound errors are perceived by the listener as clear-cut substitutions of
one phoneme segment for another, (b.) they typically occur in
single segments, and (c.) if an erroneous segment is temporally shifted, it is well-formed (Fromkin, 1971; Shattuck-
194
c o r t e x 7 5 ( 2 0 1 6 ) 1 9 3 e2 0 3
Hufnagel, 1987; Shattuck-Hufnagel & Klatt, 1979). The separation of the phonological encoding level from the phonetic or
articulatory implementation level (Dell, 1986; Dell, Juliano, &
Govindjee, 1993; Levelt, Roelofs, & Meyer, 1999) resulted in
articulatory implementation being viewed as essentially independent of phonological encoding processes.
Research focusing on speech production deficits of aphasic
patients has similarly used the construct of the psychological
reality of phonemes and features in the attempt to elucidate
error types in aphasic speech. In particular, the phoneme errors produced by both anterior and posterior aphasics have
been viewed as including the addition, deletion, substitution,
or incorrect sequencing of one or more phonemes within a
word. Both patients with anterior lesions, clinically diagnosed
as Broca's or non-fluent aphasics, and patients with posterior
lesions, clinically diagnosed as Conduction and Wernicke's
aphasics, show similar patterns: phoneme substitution errors
are the most common error type; there are more consonant
than vowel errors; and more single feature substitutions occur
than multiple feature substitutions (Blumstein, 1973; Burns &
Canter, 1977; Haley, Jacks, & Cunningham, 2013; Halpern,
Keith, & Darley, 1976; Lecours & Lhermitte, 1969). These
phoneme errors in aphasic populations are subsumed under
the category of phonemic or literal paraphasias.
Despite similarities in phonological errors, anterior and
posterior aphasics have been differentiated in the aphasia
literature on the basis of the presence (or absence) of phonetic
errors (for review see Blumstein, 2000). While posterior
aphasics have been described as having fluent speech with
multiple phonemic paraphasias, the speech of anterior
aphasics has been characterized as slow, labored, with phonetic distortions and initiation difficulties. The occurrence of
phonetic distortions is not systematic in that they do not
appear in every utterance nor do they routinely occur in the
same phonemes.
Importantly, acoustic analyses of speech production deficits in anterior aphasics have shown that despite articulatory
output deficits, the patients maintain the underlying phonological distinctions. In particular, although anterior aphasics
have shown deficits in the production of voice-onset time
(VOT), a temporal cue distinguishing voiced and voiceless stop
consonants (Blumstein, Cooper, Goodglass, Statlender, &
Gottlieb, 1980; Blumstein, Cooper, Zurif, & Caramazza, 1977;
Freeman, Sands, & Harris, 1978; Gandour & Dardarananda,
1984; Itoh, Sasanuma, Hirose, Yoshioka, & Ushijima, 1980;
Shewan, Leeper, & Booth, 1984), they can appropriately
implement the voiced-voiceless distinction in the production
of word final voiced and voiceless stop consonants utilizing
the duration of the preceding vowel (Baum, Blumstein,
Naeser, & Palumbo, 1990). Similarly, anterior aphasics have
shown impaired production of voiced fricatives (Baum et al.,
1990; Harmes et al., 1984). However, Kurowski, Hazen, and
Blumstein (2003) found that these patients were able to coordinate the articulatory gestures for voicing to distinguish
voiced and voiceless fricatives, but exhibited abnormal glottal
patterning in voiced fricatives due to weak glottal excitation.
In summary, it may be said that, in the aphasia literature,
there has been an established dichotomy between phonological selection/planning deficits characteristic of posterior
aphasics and articulatory implementation deficits characteristic of anterior aphasics (see Blumstein, 2000, for a review).
Nonetheless, it is worth noting that, even in the context of
this dichotomy, anterior aphasics do make phonemic paraphasias, suggesting that they too display phonological selection and planning deficits (Blumstein, 1973; Haley et al., 2013),
and posterior aphasics show phonetic changes in their speech
output, suggesting that they have subtle articulatory implementation deficits (Baum et al., 1990). Taken together, these
findings suggest that some phonemic paraphasias reflect
phonetic (articulatory) rather than phonological (selection)
impairments, consistent with the view that the processes
involved in phonological selection/planning and articulatory
implementation stages may not be as independent as suggested in the literature, but rather they are inextricably linked.
Indeed, in a series of review papers, Buckingham
(Buckingham, 1986; 1992a; Buckingham & Yule, 1987) challenged the view that phonemic paraphasias were clear-cut
substitutions. Rather, he proposed that many phonemic paraphasias were what he called ‘phonemic false evaluations,’
whereby the speaker produced a phonetically distorted target
phoneme that was subsequently misperceived by the listener.
In his argument, Buckingham (Buckingham & Yule, 1987)
referred to the results of several studies suggesting that both
anterior and posterior aphasics showed articulatory impairments in the production of target phonemes (Blumstein et al.,
1980; Tuller, 1984).
Indeed, in the last two decades, a number of instrumental
studies of normal speech has provided evidence against the
simple division of speech errors into phonological versus
phonetic categories that had been based primarily on transcription evidence. Boucher (1994) showed in X-ray films of
target and speech error tokens intermediate articulations as
evidenced by tongue overshoot and undershoot in wordinitial consonants. Mowrey and MacKay (1990), using electromyographic recordings to observe speech motor activity in
a tongue twister task, found that one third of the tokens
showed intermediate articulations between the error and the
target (i.e., two motor patterns produced at the same time) as
well as graded (sub-phonemic) motor activity which in some
cases resulted in an intermediate percept. They claimed that
their results supported Laver's (1980) hypothesis that induced
vocalic errors including both English and non-English diphthongs might originate from the speaker's indecision, sending
neuromuscular commands simultaneously for two canonical
forms resulting in an intermediate vowel. Mowrey and
MacKay (1990) suggest further that models of speech production need to provide for “parallel” processing of two
structures to the level of motor specification, allowing for
“simultaneous and graded execution” (p. 1310).
The issue of gradient errors and the output stage they
originate from has become a focus in the more recent speech
error literature. Using the SLIP technique (Spoonerisms of
Laboratory Induced Predisposition) to elicit speech errors,
Pouplier (2007) applied articulography to examine intrusion
and reduction speech errors which were described as “errors
in phasing between the interacting consonant gestures” (p.
311) and concluded that her data showed “a gestural intrusion
bias, leading to the simultaneous production of the intended
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and an intruding errorful consonant gesture” (p. 336) (see also
€ ller, Jansma, Rodriguez-Fornells, & Münte, 2007).
Mo
Using the gestural model, Goldstein, Pouplier, Chen,
Saltzman, and Byrd (2007) elicited speech errors in a repetition task and analyzed them kinematically (cf. also Pouplier,
Chen, Goldstein, & Byrd, 1999). Goldstein et al. speculated
that “gradient gestural errors (subsegmental)… are occurring
at the speech planning level rather than purely at the level of
low-level articulatory execution” (p. 408). Using acoustic analyses of fricative voicing, duration, and amplitude, Frisch and
Wright (2002) focused on word-initial [s] and [z] in tongue
twisters. Their results were consistent with the view that
speech errors reflected a gradient phonetic level with lowlevel components of individual phonetic features being distorted. These low-level errors would be potentially classified
as articulatory and not phonological in nature. They also
pointed out that, in order to account for these gradient speech
errors, speech production models must include processes of
activation and competition among phonetic articulatory
plans.
One of the models that specifically includes both activation
and competition among articulatory plans is the cascading
activation model (Goldrick, 2006; Goldrick & Chu, 2014; Rapp &
Goldrick, 2000). This model allows an earlier lexical processing
stage to generate multiple lexical representations including
the target word and potential lexical competitors. These
competing representations are sent downstream with their
corresponding phonological representations partially activated. In cases where there remains partial activation of both
the target word and competitor, articulatory implementation
reflects phonetic properties of both representations.
Basing their study within the framework of cascading
activation, Goldrick and Blumstein (2006) explored the relationship between phonological planning and articulatory
processes by inducing speech errors using tongue twisters
that focused on word-initial [k] and [g] (see also McMillan &
Corley, 2010). Acoustic analysis of VOT in these stop consonants revealed traces of the target token in the VOT durations
of error tokens: that is, when compared to their non-tongue
twister baseline productions, the VOT of target voiced tokens were longer and the VOT of target voiceless tokens were
shorter. These traces were hypothesized to be the result of
cascading activation of the phonological representations of
competing lexical candidates to articulatory processes.
The hypothesis that there is co-activation and hence
competition between lexical candidates is an inherent property of Dells' model of spoken word production (1986). Here,
interactive spreading activation occurs between lexical and
phonological levels, with activation spreading from word
units to lower level constituent phonemes, and activation of
these lower level constituents in turn feeding back to the
lexical level. As a result, the activation of a target word is
increased by the activation of its phonological neighbors (cf.
also Dell & Gordon, 2003). The greater the number of neighbors, the more likely the target word will be selected and
encoded correctly at the phonological level.
Applying this framework to lexical access in aphasia,
Gordon (2002) showed that the extent of competition among
words in the lexicon influences access to target lexical candidates. In particular, the occurrence of paraphasic errors in
195
aphasia was influenced by neighborhood density; the greater
the number of phonologically similar words, the fewer
phonological errors made by the aphasic participants. While
these findings support the view that the co-activation of lexical candidates influences lexical access in aphasia (cf. also
Dell, Schwartz, Martin, Saffran, & Gagnon, 1997), it remains
unclear whether co-activation of lexical candidates cascades
to and influences articulatory processes in aphasic speech,
and hence whether acoustic traces would be found in the
production of a phonological paraphasia.
It is the goal of the current study to examine this question.
In particular, we investigated whether phonemic paraphasias
arise from: a). a mis-selection and planning of phonemic
units, as traditionally proposed, b). a combination of misselection and planning of phonemic units and articulatory
(phonetic) impairments, as proposed by Buckingham (1986;
1992a; Buckingham & Yule, 1987), or c). the co-activation of a
target and competitor resulting in speech output that has
some phonetic properties of both. To this end, syllable-initial
voiced and voiceless fricative consonants, [z] and [s], were
produced in CV syllables by both anterior and posterior
aphasics. Acoustic analyses were conducted focusing on two
acoustic parameters signaling voicing in fricative consonants:
duration and amplitude properties of the fricative noise
(Crystal & House, 1988: Stevens, Blumstein, Glicksman, Burton
& Kurowski, 1992).
Our hypothesis is that paraphasias will show acoustic
‘traces’ of the target stimulus, i.e., voiceless paraphasias,
[z] / [s*], will be more [z]-like, and voiced paraphasias, i.e.,
[s] / [z*], will be more [s]-like. Additionally, we hypothesize
that both anterior and posterior aphasics will show similar
patterns of performance, challenging the strict dichotomy in
the aphasia literature claiming that posterior aphasics have
phonological selection/planning deficits and anterior aphasics
have articulatory implementation deficits. Such findings have
important implications for the nature of speech output deficits in aphasia, for they suggest that phonemic paraphasias
arise not from phonological selection stages, but result from
co-activation of representations which ultimately influence
articulatory implementation.
2.
Method
2.1.
Subjects
Seven aphasic subjects participated: three Broca's aphasics (2
male, 1 female), three Conduction aphasics (2 males, 1 female), and one Wernicke's aphasic (male). These patients
were recruited from the Harold Goodglass Aphasia Research
Center at the Boston VA Medical Center (n ¼ 2) as well as from
various Rhode Island hospitals: the Providence VA Medical
Center (n ¼ 2), Roger Williams Medical Center (n ¼ 2), and
Memorial Hospital (n ¼ 1). All of the subjects were righthanded, native speakers of English. Aphasia diagnosis was
made on the basis of clinical examination using the Boston
Diagnostic Aphasic Examination (BDAE) (Goodglass & Kaplan,
1983). Table 1 provides the BDAE scores for overall fluency,
articulation, and auditory comprehension, in addition to a
description of the lesion localization for each patient.
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Table 1 e Clinical and lesion profile of aphasic patients (B ¼ Broca's, C ¼ Conduction, and W ¼ Wernicke's aphasia).
Subj.
Gender
Age at
testing
Time post
onset
BDAE subtests
Lesion
B1
Female
58
13 yrs.
Fluency ¼ þ.58
Aud Comp ¼ þ.95
Articulation ¼ 50%
Large left insular lesion extending to anterior temporal lobe, sparing both
Wernicke's area and the anterior region of Broca's area.
B2
Male
57
15 yrs.
Fluency ¼ þ.55
Aud Comp ¼ þ.96
Articulation ¼ 45%
Involvement of the entire lenticulostriate artery distribution of the MCA
territory including the left caudate nucleus, globus pallidus, and the
intervening anterior internal capsule. The infarct extends laterally to
involve the medial temporal cortex and insula and superiorly to involve the
PVWM on the left anteriorly. Lucency encroaches upon the posterior limbic
internal capsule. The lesion involves the anterior temporal lobe but not
mesial temporal structures. There is a separate small lesion in the area of
the sub-thalamic nucleus and spinol-thalamic tract; the lesion spares
Broca's and Wernicke's areas. Low density in the entire region between
Broca's and Wernicke's areas from subcortical through insula and into
temporal cortex.
B3
Male
74
25 yrs.
Fluency ¼ þ.40
Aud Comp ¼ þ.77
Articulation ¼ 40%
Left frontal lesion involving the posterior half of Broca's area and most of
the middle frontal gyrus with deep extension to the border of the left frontal
horn. The lesion involves the head of the caudate and anterior limb of the
internal capsule. It extends superiorly into the pre-motor, motor and
sensory cortex areas and the white matter deep to these areas including the
periventricular white matter adjacent to the body of the left lateral ventricle
and undercutting fibers of the supplementary motor area. There is a clip in
the anterior communicating artery.
C1
Male
57
2 yrs.
Fluency ¼ þ.64
Aud Comp ¼ þ.52
Articulation ¼ 60%
Left posterior temporoparietal lesion involves the insula and 1/4 of
Wernicke's area with superior extension into the supramarginal and
angular gyrus areas and the white matter deep to them. The lesion
continues up into the superior parietal lobule. There is slight bilateral
frontal atrophy.
C2
Female
88
1 yr.
Fluency ¼ þ.61
Aud Comp ¼ þ.84
Articulation ¼ 60%
New left posterior temporoparietal infarct post left craniotomy for chronic
bifrontal subdural hematoma (R > L).
Small left hemisphere lesion in the white matter deep to the posterior
portion of the middle temporal gyrus and deep to the posterior half of
Wernicke's area. There are also multiple scattered high signal intensities
throughout the white matter bilaterally. There are also bilateral subdural
hematomas present. In the right hemisphere, the subdural is very large and
is present along the entire convexity from anterior (frontal) to posterior
(occipital). On the left, the subdural is present in the frontal and parietal
regions.
C3
Male
66
1 yr.
Fluency ¼ þ.64
Aud Comp ¼ þ.53
Articulation ¼ 65%
Left temporo-parietal lesion involving a little less than half of Wernicke's
area with superior extension into the supramarginal and angular gyri and
the white matter deep to these areas. The lesion is in part of Wernicke's area
but in all of SMG. No Broca's area involvement. No evidence of hemorrhage.
There is moderate atrophy.
W1
Male
73
2 yrs.
Fluency ¼ þ.66
Aud Comp ¼ #1.65
Articulation ¼ 60%
Large focal area of low attenuation in the left fronto-parietal area consistent
with subacute cortical infarct in L MCA.
2.2.
Stimuli
The target stimuli consisted of CV syllables: an initial alveolar
fricative consonant [s, z] followed by one of five vowels [i e a o
u]. These CV syllables were spoken in two experimental conditions: isolation and context. In the isolation condition, the
target CV syllables were produced in citation form. This condition provided a means for examining productions independent of context and then to explore potential differences
in initial consonant production as a function of the preceding
context. Every fricativeevowel combination occurred once in
each of eight separately randomized blocks of tokens, yielding
a total of 80 token trials.
In the context condition, the CV syllables were spoken in
two carrier phrases (“Please speak _ again”; “Say a big _
again”), which allowed for examination of potential changes
in voicing of fricative consonants as a function of the voicing
of the preceding consonant. The context condition was also
employed to reduce difficulties in initiating speech often
encountered by Broca's aphasics. Every combination of carrier
phrase and CV target appeared once in each of eight randomly
ordered blocks of sentences, yielding a total of 160 tokens.
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197
(The context condition results are reported in the
Supplementary Materials).
The stimuli were printed in orthographic form on 3 $ 5
cards which the subjects were instructed to read, speaking
naturally. If a subject was unable to produce the target syllable
by reading the card, the experimenter read the token aloud
and asked the subject to repeat it. If the patient was unable to
repeat the full sentence context, it was reduced to “Speak __”
and “Big __”. Tokens that the subject could not produce were
presented once more at the end of the stimulus block. Short
breaks were provided at the end of each block and as needed.
Given that the goal of this study is to examine whether the
acoustic properties of paraphasic errors show a ‘voicing’ trace
of the intended consonant target, acoustic analyses were
performed only on those utterances that were perceived by
the examiners as either exemplars of the target CV syllable or
as exemplars of a voicing paraphasia [s] / [z*] or [z] / [s*].
Thus, utterances in which the patient made other types of
paraphasias on the CV target syllable (including the vowel)
were excluded from analysis. All of the analyzed tokens were
labeled as to whether a paraphasia occurred on the patient's
first attempt or second attempt to produce the target syllable.
The first and second attempt utterances were analyzed
separately for the following reason. It was unclear whether a
second attempt reflected a failure to produce the originally
presented target, or the influence of the production or
perception of the initial first attempt on the second attempt by
the participant. Hence, the ‘source’ of the paraphasia in the
second utterance may not have been the same as that of the
first utterance [cf. also Buckingham (1992a) for a similar view
in considering multiple attempts or conduite d'approche
produced by Conduction aphasics]. For this reason, we report
only the results of the first utterance.
In total, there were 95 first attempt voicing phonemic
paraphasias produced by the Broca's aphasics (B1 ¼ 14;
B2 ¼ 35; B3 ¼ 46), 106 produced by the Conduction aphasics
(C1 ¼ 35; C2 ¼ 28; C3 ¼ 43), and 13 by the one Wernicke's
aphasic. With respect to second attempt voicing paraphasias,
there were 80 produced by the Broca's aphasics (B1 ¼ 19;
B2 ¼ 30; B3 ¼ 31), 67 produced by the Conduction aphasics
(C1 ¼ 20; C2 ¼ 9; C3 ¼ 38), and 11 by the Wernicke's aphasic.
emergence of the harmonic spectrum of the following vowel,
and by an increase of at least 10 dB in spectral energy at or
above 2 kHz. Again, both LPC and DFT analyses were conducted using a 15 msec full-Hamming window to make this
determination. In addition, a drop of at least 10 dB in the
5e10 kHz frequency range was used to confirm the cessation
of frication noise.
Given the production difficulties inherent in aphasic
speech, epenthetic vowels and other forms of vocal cord activity sometimes preceded the onset of frication. In these
cases, the vocalic activity was not included as part of the
fricative duration unless there was co-occurring frication
noise evident in the waveform of the vocalic activity, as
determined by the criteria described above. In addition, the
vocalic activity with co-occurring frication had to be contiguous with the syllable waveform.
Utilizing the two fricative endpoint cursors, the acoustic
parameters of fricative duration and amplitude difference
were measured in the tokens. Fricative duration was
measured as the time interval (in msec) between the fricative
cursors in each alveolar consonant in the isolation and
context conditions. The amplitude parameter measured the
amplitude of the first harmonic (H1) as determined by DFT
analysis in the fricative noise interval relative to that of the
vowel onset. Prior research (Pirello, Blumstein, & Kurowski,
1997; Stevens et al., 1992) showed that voiced fricatives displayed a 10 dB difference or less between the fricative and
vowel that was sustained over at least 30 msec over the frication noise (i.e., three consecutive 30-msec windows
advanced in 10 msec intervals during the frication noise
duration), and voiceless fricatives displayed greater than a
10 dB difference between the amplitude of the fricative noise
interval and the following vowel. In the present study, the
amount and extent of glottal excitation as determined by H1
was charted throughout the duration of the fricative noise
using a 30-msec full-Hamming window which was advanced
in 10-msec steps across the entire frication interval. The
overall mean and standard deviation of the amplitude differences obtained across the fricative duration was determined
for each token.
2.3.
3.
Procedure
Stimuli were recorded using a Sony Walkman Professional
tape recorder and a Sony stereo microphone. The recorded
stimuli were then digitized at a sampling rate of 20 kHZ with a
9.0-kHZ lowpass filter (Butterworth 24 dB/octave), and a 12 bit
quantization.
To analyze the acoustic parameters in the fricative noise,
cursors were set at the onset and offset of the fricative noise
using a software waveform editor (Mertus, 2000). Frication
was acoustically defined as the presence of high frequency
noise in the range between 5 and 10 kHz. Using a 15 msec fullHamming window, the onset cursor was placed at the earliest
position on the waveform at which DFT and LPC analyses
showed an increase of at least 10 dB within the high frequency
range (5e10 kHz) when compared to the background noise
level. The offset of frication noise was determined by the
absence of high frequency noise in the waveform, the
Results
As indicated earlier, paraphasic utterances were classified and
analyzed in terms of whether they were the first or second
attempt to produce the target. Discussion of the results will be
limited to only the first paraphasic error that the patient
produced.
3.1.
Duration measure
Fig. 1 shows the overall mean duration of the fricative noise
collapsed across vowel ([i e a o u]) and conditions (isolation
and the 2 context conditions) for the correctly produced
(baseline) and paraphasic [z] and [s] productions for the Broca's (n ¼ 3), Conduction (n ¼ 3), and Wernicke's aphasics (n ¼ 1).
(The Wernicke's aphasic did not make any [s] / [z*] paraphasic errors). The baseline tokens indicate that for all groups,
similar to normals, the duration of the voiceless fricative [s] is
Dura on (ms)
198
c o r t e x 7 5 ( 2 0 1 6 ) 1 9 3 e2 0 3
300
250
200
150
100
50
0
[s]
Table 2 e Mean duration measures (in msec) across the five
vowels and three conditions (isolation, [k]-context, [g]context) for the baseline and paraphasic productions for
each subject.
[s] →[z*]
Aphasia type
[z]
Broca
[z] →[s*]
Subjects
[z]
[s / z*]
[s]
[z / s*]
B1
B2
B3
115
137
188
147
136
152
216
168
215
212
261
228
184
204
209
199
C1
C2
C3
191
157
155
168
208
143
181
178
269
225
247
247
237
208
229
230
W1
154
e
239
200
Mean
Conduction
Fig. 1 e Duration of the fricative noise (in msec) for baseline
(correctly produced) [s] and [z] tokens and [s] / [z*] and
[z] / [s*] phonemic paraphasias produced by participants
clinically diagnosed with Broca's, Conduction, and
Wernicke's aphasia.
longer than that of the voiced fricative [z]. Importantly, the
paraphasic errors for all groups show an acoustic trace of the
original target; that is, the [s] / [z*] paraphasias are longer in
duration than the baseline [z], and hence are more [s]-like, and
similarly, the [z] / [s*] paraphasias are shorter than the [s]
baseline, and hence are more [z]-like.
Although the pattern of the overall data suggests that the
paraphasic errors reflect a trace of the original target, there
were too few subjects per group to conduct statistical analyses.
Moreover, it is not clear from the means whether all subjects
within a group showed this pattern. For this reason, we conducted two sets of additional analyses. In the first, we examined whether the overall pattern across all of the participants
was statistically reliable. We then analyzed each subject's
production data individually to determine whether the pattern
of responses for that subject reflect acoustic traces.
A one-way within-subjects parametric analysis of variance
(ANOVA) was conducted to examine whether there were
reliable differences across conditions (baseline [s], baseline [z],
paraphasic [z] / [s*], and paraphasic [s] / [z*]). Assumptions
of normality and homogeneity of variance were satisfied as
shown by Mauchly's test for sphericity (p > .05). Results of the
ANOVA showed a significant effect [F(3, 18) ¼ 71.233, p < .0001].
Post-hoc Duncan pair-wise t-tests using the Bonferroni
correction for multiple comparisons (p < .0083) revealed statistically significant differences between all conditions, except
for the [z] versus [s] / [z*] comparison (p < .02). Thus, on
balance, considering the aphasic patients as a group, phonemic paraphasias contained an acoustic trace of their original
target: the trace of a target [s] lengthens the fricative duration
of the [z] error, while the trace of a target [z] shortens the
fricative duration of the [s] paraphasia.
The individual data for the aphasics is shown in Table 2. As
can be seen, similar to normals, all patients showed longer
baseline voiceless fricative tokens than baseline voiced fricative tokens. With respect to the [s / z*] voicing paraphasias,
the mean durations indicate that a [z] produced instead of the
intended target [s] was longer than the baseline [z] for all
subjects except C2. For [z / s*], the [s] produced when the
intended target was a [z] had a shorter mean duration than
that of the baseline [s] for all subjects.
Mean
Wernicke
To evaluate whether the error tokens produced by each
aphasic subject showed statistically reliable evidence of traces
of the target, separate Wilcoxon (signed rank sum test) analyses were performed on duration values for each subject,
pairing individual target and error productions. In these
paired analyses, the target and error tokens were matched for
vowel and condition (isolation, /k/context, /g/context). A
minimum of five matched pairs of tokens were used in performing the Wilcoxon analysis on each error type ([s] / [z*];
[z] / [s*]). Because there were often fewer than 5 matched
tokens (i.e., tokens that shared vowel context in the same
condition in the isolation and [k] and [g] context conditions),
the matched tokens for each error type were combined across
isolation and context conditions.
Each of the error tokens was paired with both a correctly
produced baseline [s] and [z] token in order to determine if the
error token was significantly different from both the target
and the baseline tokens that matched the error production.
For example, if the paraphasic error was [s] / [z*], then this
[z*] should be different in duration from the target [s], since it
was perceived as a [z]. The more critical question is whether
the paraphasic [z*] is significantly different from a baseline [z]
in duration, indicating the presence of a trace of the target [s].
The left half of Table 3 shows the Wilcoxon results for duration. With the exception of patients C1 and C2, each aphasic
showed significant changes in the duration of the fricative
noise when producing a paraphasic error, thus showing the
presence of an acoustic trace in their voicing paraphasias.
3.2.
Amplitude measure
Fig. 2 displays the group mean amplitude differences for
baseline (correctly produced target) fricatives and for the
voiced ([s / z*]) and voiceless ([z / s*]) paraphasias collapsed
across vowels and context conditions. (The Wernicke' aphasic
did not make any [s] / [z*] paraphasias). For each group of
patients, the baseline [s] and [z] amplitude measure shows, as
do normals, smaller amplitude differences between the
amplitude of the fricative noise and the vowel for the [z] target
tokens compared to the [s] target tokens. Critically, there is an
acoustic trace of the target in the paraphasias; [s] / [z*] paraphasias show an increase in the amplitude parameter
199
c o r t e x 7 5 ( 2 0 1 6 ) 1 9 3 e2 0 3
Table 3 e Wilcoxon results for the duration and amplitude
comparing the paraphasic error to the baseline that
corresponded to it. For [s] / [z*], the corresponding
baseline is [z]; for [z] / [s*], the corresponding baseline is
[s]. An asterisk (*) in the cell indicates a statistically
significant result; a minus sign (¡) indicates a nonsignificant result. Blank indicates that there were too few
paraphasic tokens (or none) to perform a statistical
analysis.
Subjects
Duration measures
Amplitude measures
[s / z*]
[z / s*]
[s / z*]
[z / s*]
*
e
e
*
*
B1
B2
B3
*
*
*
C1
C2
C3
e
*
W1
e
e
*
*
*
*
*
*
*
*
Amplitude (dB)
rendering the [z*] more [s]-like, and conversely, [z] / [s*]
paraphasias show a decrease in amplitude rendering the [s]
paraphasias more [z]-like.
Further analyses were conducted analogous to those carried out on the duration measures. A one-way ANOVA,
collapsing across the 3 patient groups (Broca, Conduction, and
Wernicke), vowel, and context conditions, examined whether
the overall amplitude effects were statistically reliable.
Similar to the duration analysis, assumptions of homogeneity
of variance were satisfied. Results of the ANOVA showed a
significant effect F(3, 18) ¼ 18.455 (p < .0001). Post-hoc pairwise
t-tests using the Bonferroni correction for multiple comparisons (p < .0083) revealed statistically reliable differences only
for the [z] versus [s] and the [s] versus [s] / [z*]. The remaining
comparisons showed the following significance levels: [z]
versus [z] / [s*], p < .01, [s] / [z*] versus [z] / [s*], p < .024,
and [z] versus [s] / [z*] and [s] versus [z] / [s*] p < .066.
The individual amplitude data for each patient is shown in
Table 4. Similar to normals, all patients showed a smaller
amplitude difference between the first harmonic in the
40
30
20
[z]
10
[s] → [z*]
0
[s]
[z] → [s*]
Fig. 2 e Amplitude measure of voicing (in dB) for baseline
(correctly produced) [s] and [z] tokens and [s] / [z*] and
[z] / [s*] phonemic paraphasias produced by participants
clinically diagnosed with Broca's, Conduction, and
Wernicke's aphasia.
Table 4 e Mean amplitude measures (in dB) across the five
vowels and three conditions (isolation, [k]-context, [g]context) for the baseline and paraphasic productions for
each subject.
Aphasia type
Broca
Subjects
[z]
[s / z*]
[s]
[z / s*]
B1
B2
B3
17
9
15
13
14
9
24
16
29
39
39
35
16
12
37
22
C1
C2
C3
11
12
13
12
12
24
22
19
41
37
26
35
36
35
24
31
W1
16
e
33
31
Mean
Conduction
Mean
Wernicke
fricative noise and the vowel for the voiced fricative [z]
compared to the voiceless fricative [s]. With respect to the
paraphasic errors, all patients showed an acoustic trace in the
[z] / [s*] paraphasia, with the paraphasic [s*] showing a
decrease (and hence more voicing) in the amplitude measure
compared to the correctly produced [s]. Evidence for a trace in
the [s] / [z*] paraphasias was weaker, failing to emerge for 2
of the 3 Broca's aphasics (B1 and B2) and showing only a 1 dB
difference for C1.
Wilcoxon analyses of the individual subject data were
conducted following the same procedures as those done for
the duration measure by matching individual target and error
productions across vowel and condition. The right portion of
Table 3 shows the results. With the exception of B1 and B2,
each aphasic showed evidence of an acoustic trace in his/her
paraphasias in the amplitude measure. Neither C2 nor W1 had
the minimum number of matched token pairs for [s] / [z*]
paraphasias to perform the Wilcoxon analysis.
4.
Discussion
The results of this study show that the production of phonemic paraphasias in aphasic patients leaves an acoustic trace
of the target phoneme. In particular, although voicing paraphasias in fricative consonants were both perceptually and
acoustically distinct in voicing from their target (and hence
were paraphasic errors), the acoustic manifestation of these
paraphasias contained a voicing ‘trace’ of the original target;
[s] paraphasias were more [z]-like, and [z] paraphasias were
more [s]-like. Thus, although an [s] / [z*] paraphasia was
produced as a [z], and acoustically it was voiced, it was more
‘voiceless’ (as shown by both duration and amplitude measures of voicing) than correctly produced [z] tokens. Similar
effects emerged in voiceless fricative paraphasias. These
findings indicate that phonemic paraphasias are not clear-cut
substitutions of one phoneme for another reflecting the selection of an incorrect phoneme which is then implemented
correctly nor are they a combination of some phonemic substitutions and other articulatory (phonetic) implementation
errors. Instead, acoustic properties of the original target are
manifested in paraphasic productions.
200
c o r t e x 7 5 ( 2 0 1 6 ) 1 9 3 e2 0 3
Importantly, all aphasic patients, regardless of clinical
diagnosis or lesion localization showed this effect. Considering the clinical diagnosis, the classical aphasic literature
made a distinction between the speech output of anterior and
posterior aphasics. Anterior aphasics were characterized as
having articulatory implementation impairments, and posterior aphasics were characterized as having selection impairments. Within the posterior aphasias, phonemic paraphasias
are a clinical feature of Conduction aphasics (Pradat-Diehl,
Tessier, Vallat, Mailhan, et al. (2001)). Although Wernicke's
aphasics produce them as well, their occurrence is much less
frequent (Goodglass & Kaplan, 1983). Nonetheless, despite
these clinical distinctions, traces appeared in the paraphasic
productions across the aphasia syndromes.
As to lesion localization, examination of the lesion localization across patients (as shown in Table 1) reveals an
extensive pattern of lesions including frontal, parietal, and
temporal lobes as well as subcortical areas. And as has been
shown in earlier research, a clinical diagnosis of Broca's
aphasia does not always require a lesion in Broca's area (the
inferior frontal gyrus) (Willmes & Poeck, 1993). Indeed, only B3
showed a lesion in this area. There is insufficient data to
determine whether damage to particular neural areas would
fail to show evidence for traces in phonemic paraphasias.
Suffice to say, the large number of neural areas damaged
across the patients studied suggests that the presence of
acoustic traces in phonemic paraphasias may be pervasive in
aphasia irrespective of lesion.
It is the case that depending upon the acoustic parameter
there were differences across the patients in the extent to
which traces emerged. For example, the amplitude measure
failed to show evidence of traces for 2 of the 3 Broca's aphasics
(B1 and B2). These findings are not surprising given that prior
research has shown that Broca's aphasics exhibit weak glottal
excitation in the production of fricative consonants compared
to normal controls (Kurowski et al., 2003). As a consequence, a
measure relying on amplitude differences within an utterance
(amplitude of the fricative noise relative to the amplitude of
the vowel) was likely not sensitive enough to pick up traces in
two of the Broca's aphasics.
With regard to the duration measure, two of the three
Conduction aphasics (C1 and C2) failed to show this acoustic
trace, although they did use duration to distinguish correctly
produced voiced and voiceless target productions. Previous
research has shown deficits in posterior aphasics including
Conduction aphasics in the production of a number of duration parameters of speech including fricatives (Baum et al.,
1990). These same patients, however, do not show deficits in
laryngeal control. As a result, it is not surprising that a duration parameter failed to show evidence of traces for the two
Conduction aphasics while acoustic traces emerged in their
data using the amplitude measure.
The presence of acoustic traces in phonemic paraphasias
challenges the traditional explanation for the basis of these
errors. That is, they do not reflect the selection of the wrong
phoneme followed by its correct articulatory implementation.
Rather, it appears as though the presence of acoustic traces
reflects the selection and co-activation of both the target and
voicing competitor which are ultimately sent downstream to
articulatory processes. As described earlier, current models of
spoken word production propose that the selection of a lexical
(or syllable) candidate activates not only the target but also
competitors which share either sound structure or semantic
properties (Dell, 1986; Dell et al., 1997; Rapp & Goldrick, 2000).
Under normal circumstances, the production of the target
phoneme requires that the correct phonological segment and
its features be activated and competitors be inhibited. Phonemic paraphasias appear to arise from the activation of the
phonological representation of both the target and
competitor.
There are two possible processes that may give rise to the
paraphasia and trace. One possibility is that the incorrect
segment is selected along with reduced activation of the target
phoneme resulting in the incorrect production and a trace of
the target. Alternatively, the correct segment is selected and
there is overactivation of the competitor resulting in the
production of the incorrect segment and a trace of the intended target. While we cannot distinguish between these two
possibilities on the basis of the current data, we favor the first
alternative since it is consistent with the findings of recent
research suggesting that aphasic participants show a lexical
access impairment characterized by a failure to resolve lexical
competition (Blumstein, 2011; Yee, Blumstein, & Sedivy, 2008).
Here, it has been proposed that aphasics fail to inhibit competitors owing to a deficit in which representations are weakly
activated, or a deficit in which they cannot sufficiently inhibit
partially activated representations.
That traces occur across all patients is consistent with the
view that the neural substrates underlying spoken word production are broadly distributed and the functional architecture of this system reflects cascading processes. Consistent
with this is evidence from both the aphasia and functional
neuroimaging literature.
Past research examining the acoustic substrates of speech
production in aphasia has shown that not only do anterior
aphasics display articulatory deficits but posterior aphasics
also display a subtle phonetic impairment affecting a range of
phonetic parameters (cf. Blumstein, 2000, for review). In the
latter case, the impairments are not evident in the patient's
productions but are only revealed with instrumental analyses
of speech output (cf. Baum et al., 1990; Vijayan & Gandour,
1995). Given the current study, what is less clear is the basis
of the deficits that had been proposed. For example, in a series
of studies conducted in the 70's and 80's investigating the
production of voicing in stop consonants in Broca's, Conduction, and Wernicke's aphasics (Blumstein et al., 1980, 1977;
Gandour & Dardarananda, 1984), VOT measures were taken
of target productions independent of their perception. Thus, the
VOT value for a particular target was measured whether it was
perceived as a voiced or voiceless consonant. Results showed
three types of productions: those that fell within the expected
range for a voiced and voiceless stop consonant and were
assumed to be normal productions, those that fell within the
range of the contrasting phonetic category (the VOT of a [t]
target fell within the VOT range of the [d] category) and
assumed to be phonemic paraphasias, and those that fell between the two voiced and voiceless phonetic categories and
assumed to be articulatory implementation errors. All 3
groups made both types of errors, although the Wernicke's
aphasics made considerably fewer errors. It is possible that
c o r t e x 7 5 ( 2 0 1 6 ) 1 9 3 e2 0 3
many of these productions actually reflected traces of the
original target rather than, as originally proposed, two distinct
types of errors.
Looking at fMRI findings, evidence suggests that spoken
word production recruits a broadly distributed neural system
(Indefrey & Levelt, 2004), and activation patterns within this
system support models of cascading activation. Using the
presence or absence of minimal pair voicing contrasts as a
proxy for lexical density, behavioral results show longer VOT
values for words beginning with voiceless stop consonants
that have voiced minimal pairs compared to words that do not
(e.g., tense-dense vs tenth, *denth is not a word) (Baese-Berk &
Goldrick, 2009; Fox, Reilly, & Blumstein, 2015). Peramunage,
Blumstein, Myers, Goldrick, and Baese-Berk (2011) examined
the neural substrates of this lexically conditioned phonetic
variation and showed cascading activation throughout the
spoken word production system with modulatory effects
under these conditions in the posterior superior temporal and
supramarginal gyri (implicated in phonological and lexical
selection), the inferior frontal gyrus (implicated in phonological planning) and the precentral gyrus (implicated in articulatory processes) (cf. also Okada & Hickok, 2006).
Taken together, the findings of the current study suggest
that phonemic paraphasias reflect the integrity of cascading
processes in spoken word production. They also suggest that
these paraphasias reflect the selection of a phonemic segment
with the concurrent co-activation of potential sound-shape
competitors, and the continued partial activation of the
competitor, resulting in the presence of a trace of the original
target segment. For such patterns to emerge requires a system
in which phonological properties of sound segments are represented in a gradient fashion rather than as binary units in
which a phonological feature is either present or absent. Of
importance, these results show unique insights from aphasia.
Whereas the presence of acoustic traces in normals emerges
using tasks that ‘stress’ the system, e.g., tongue twisters,
where the test stimuli contain the competing sound segments, such is not the case in phonemic paraphasias. Here,
the productions emerge ‘naturally’ and often, occurring under
all types of speaking conditions ranging from natural speech
to the task used in the current experiment. Thus, competition
effects that induce traces in phonemic paraphasias are clearly
intrinsic to the phonological and lexical systems being
accessed, and are neither induced nor necessarily exacerbated
by extrinsic factors.
5.
Summary
The results of this study show that phonemic paraphasias
contain an acoustic trace of the original target in the error
production and appear to derive from a common mechanism
with speech errors (c.f. also Buckingham, 1992b). The presence
of a trace of the original target suggests that there is coactivation of lexical representations in the selection of a
target word which influence downstream processes of articulation. Slips of the tongue, however, are not common, but are
typically induced by utilizing tasks such as requiring subjects
to produce tongue twisters which contain phonologically
similar, and hence, competing phonological representations.
201
In contrast, phonemic paraphasias are a common presenting
symptom in aphasia, and occur in spontaneous speech as well
as in reading and/or repeating individual words or syllables.
Importantly, unlike slips of the tongue, aphasic paraphasic
errors typically occur in the absence of competing representations present in the stimulus. Although left hemisphere
damage may exacerbate the occurrence of paraphasias, they
reflect ‘natural’ processes of speech production and cut across
clinical types of aphasia as well as lesion site.
Acknowledgments
This research was supported in part by National Institutes of
Health grants DC000314 to Brown University and P50
DC000081 to the Boston University School of Medicine. This
material is the result of work supported with resources and
the use of facilities at the Department of Veterans Affairs
Medical Centers in Boston, MA and Providence, RI. The content is solely the responsibility of the authors and does not
necessarily represent the official views or policy of the
Department of Veterans Affairs, the National Institute on
Deafness and Other Communication Disorders, or the National Institutes of Health. Thanks to Sahil Luthra for technical assistant and comments on an earlier draft of this paper.
Supplementary data
Supplementary data related to this article can be found at
http://dx.doi.org/10.1016/j.cortex.2015.12.005.
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